Generally, in animal poisoning with organophosphorus insecticides, once the acute phase of the poisoning is over, recovery is complete. In certain animals including man, however, exposure to some of the anticholinesterase organophosphorus esters results in delayed neurotoxicity. The lesions develop slowly insidiously without dramatic signs of neurologic misfunction in the beginning, and only later symptoms appear when it is most of the time too late to save or treat the subject. In early studies the clinical condition in the hen was similar to that of man, and the hen has become the animal of choice to study organophosphorus pesticides -induced delayed neurotoxicity (OPIDN). Locomotor ataxia usually develops 7-l4 days after administration, and nerve lesions are characterized by the degeneration of axons with subsequent Wallerian degeneration of myelin. Recently, leptophos, a compound which induced delayed neurotoxicity in hens, was implicated in the poisoning and paralysis of some factory workers where it was manufactured and packaged. Some scientists object to the use of the chicken as a test animal for OPIDN, and they question the validity of extrapolating from an avian species to man. The purpose of the proposed study s is to develop the cat - a species which is sensitive to OPIDN - as a practical animal model to study delayed neurotoxicity induced by organophosphorus pesticides. We propose to study the induction of OPIDN following a single and subchronic (90 days) dermal administration of EPN. We also propose a chronologic study of cats following the administration of a single dermal dose of EPN. The pharmacokinetic and metabolism of (14C)phenyl EPN will be studies in the cat. Correlations will be made between clinical condition, neurotoxic esterase, brain and plasma cholinesterases and acid phosphatase, electro-physiological parameters, histopathological changes and the accumulation, stability and metabolism of this compound in the cat.